Equis ISSN 2398-2977
Toxicity: pyrrolizidine alkaloid
Synonym(s): Ragwort toxicosis, Oral habout disease, Dunsiekte, Winton disease, Pictou disease, Suilkut disease, Schweinsberger disease
Contributor(s): Debbie Deem Morris, Nicola Menzies-Gow, Wilson Rumbeiha, Prof Alan Seawright
Introduction
- Pyrrolizidine alkaloids are toxins which mainly cause hepatotoxicity and liver failure but may also cause respiratory disease and renal damage depending on the plants involved.
- Cause: pyrrolizidine alkaloids are produced by 3 main plant families:
- Asteraceae (Senecio spp, tansy ragwort).
- Tobaceae (Crotalaria spp, rattlebox).
- Boraginaceae (Heliotropum, Amsinckia, Trichodesma and Echium spp).
- Signs: anorexia, weight loss, ventral edema, depression, icterus +/- signs of hepatic encephalopathy, eg apparent blindness, circling, head-pressing; respiratory distress.
- Diagnosis: liver function tests, hepatic biopsy, liver enzymes, alkaloids in liver, necropsy.
- Treatment: no effective specific treatment.
- Prognosis: poor if recurrent or severe.
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Pathogenesis
Etiology
- Pyrrolizidine alkaloids produced by plants.
- Ragwort (Senecio jacobea)

- contains 8 alkaloids, including retrorsine.
- Heliotrope contains several alkaloids, including lasiocarpine and heliotrine.
- Crotalaria spp contain mainly monocrotaline, some also contain fulvine and crispatine.
Predisposing factors
General
- Plants containing pyrrolizidine alkaloids are usually, but not always, unpalatable and mostly ignored.
- May be consumed when there is little alternative feed.
- Dead ragwort and other pyrrolizidine alkaloid plants, eg in hay, are more palatable.
- Repeated ingestion of small amounts over several seasons may → disease - cumulative effect.
Pathophysiology
- Pyrrolizidine alkaloids have primary toxic effect on hepatic parenchyma and secondary effects on hepatic veins, pulmonary tissues and other extrahepatic tissues such as the lungs, kidneys and heart.
- Clinical signs occur once liver damage has progressed sufficiently to compromise liver function.
- Alkaloids → primary toxic effect on liver parenchyma → megalocytosis → necrosis and inhibition of cell division.
- Reactive alkaloids crosslink DNA, impair cell division and may affect protein synthesis.
- Can interfere with copper excretion.
- Secondary toxic effect on centrilobular and hepatic veins → endothelial damage and perivascular fibrosis → vascular occlusion.
- Apparent sudden onset, often weeks after ingestion has stopped → hepatic encephalopathy Liver: hepatoencephalopathy.
Timecourse
- Usually chronic.
- Liver damage may accumulate over several years.
- Onset of clinical signs may occur several weeks to months after ingestion of plant has stopped.
Epidemiology
- Plants are not usually palatable, therefore ignored unless food is scarce.
- Dead plants, eg in hay, are readily eaten.
- Toxicity is cumulative; liver damage may occur over several seasons.
Diagnosis
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Treatment
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Prevention
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Outcomes
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Further Reading
Publications
Refereed papers
- Recent references from PubMed and VetMedResource.
- Bothia C J et al (2012) Crotalariosis equorum ("jaagsiekte") in horses in southern Mozambique, a rare form of pyrrolizidine alkaloid poisoning. J Vet Diag Invest 24 (6), 1099-1104 PubMed.
- Creeper J H et al (1999) Pyrrolizidine alkaloid poisoning of horses grazing a native heliotrope (Heliotropium ovalifolium). Aust Vet J 77 (6), 401-402 PubMed.
- Curran J M, Sutherland R J & Peet R L (1996) A screening test for subclinical liver disease in horses affected by pyrrolizidine alkaloid toxicosis. Aust Vet J 74 (3), 236-240 PubMed.
- Winter H et al (1993) Pyrrolizidine alkaloid poisoning of yaks - diagnosis of pyrrolizidine alkaloid exposure by the demostration of sulphur-conjugated pyrrolic metabolites of the alkaloid in circulating haemoglobin. Aust Vet J 70 (8), 312-313 PubMed.
- Pearson E G (1991) Liver failure attributable to pyrrolizidine alkaloid toxicosis and associated with inspiratory dyspnea in ponies - 3 cases. JAVMA 198 (9), 1651-1654 PubMed.